Lipoxin A4 suppresses the development of endometriosis in an ALX receptor‐dependent manner via the p38 MAPK pathway

Rongfeng Wu, Weidong Zhou, Shuo Chen, Yan Shi, Lin Su, Maobi Zhu, Qionghua Chen, Qingxi Chen, Qing‐Xi Chen
British journal of pharmacology · 2014 · vol. 171(21) , pp. 4927–4940 · doi:10.1111/bph.12816 · PMID:24923883 · PMC4294115 · W1507060320
article OA: bronze CC0 ⤵ 23 in-corpus citations
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Lipoxin A4 suppressed endometriosis development and progression by acting on ALX receptors to inhibit inflammation, proliferation, and invasion via the p38 MAPK pathway.

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Abstract

BACKGROUND AND PURPOSE: Lipoxins can function as endogenous 'breaking signals' in inflammation and play important roles in the progression of endometriosis. In this study, we further investigated the molecular mechanism by which lipoxin A4 (LXA4 ) suppresses the development of endometriosis. EXPERIMENTAL APPROACH: Primary endometriotic stromal cells (ESCs) were treated with IL-1β, or pre-incubated with LXA4 before incubation with IL-1β. The LXA4 receptor (ALX receptor) antagonist Boc-2 and gene-silencing approaches were used to study the involvement of the ALX receptor in anti-inflammatory signalling responses in ESCs. An animal model of endometriosis was induced in BALB/c mice by i.p. injection of an endometrium-rich fragment. KEY RESULTS: Decreased levels of LXA4 and 15-LOX-2 expression but increased expression of AXL receptors were observed in endometriotic tissues. LXA4 inhibited the release of inflammatory factors and phosphorylation of p38 MAPK in IL-1β-induced ESCs, an effect mediated by ALX receptors. LXA4 inhibited the proliferation of ESCs, as indicated by reduced DNA replication, caused G0 /G1 phase cell cycle arrest and down-regulated the expression of proliferating cell nuclear antigen in ESCs. LXA4 also attenuated the invasive activity of ESCs mainly by suppressing the expression and activity of MMP-9. In vivo, we further confirmed that LXA4 could inhibit the progression of endometriosis by acting as an anti-inflammatory. CONCLUSIONS AND IMPLICATIONS: LXA4 exerted anti-inflammatory, anti-proliferative and anti-invasive effects on endometriosis through a mechanism that involved down-regulating the activities of p38 MAPK, which was mediated by ALX receptors.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Lipoxins p38 Mitogen-Activated Protein Kinases Receptors, Lipoxin Animals Arachidonate 15-Lipoxygenase Arachidonate 15-Lipoxygenase Cells, Cultured Cytokines Cytokines Endometriosis Endometrium Endometrium Female Gene Silencing Humans Lipoxins Matrix Metalloproteinase 9 Matrix Metalloproteinase 9 Mice, Inbred BALB C

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